Abstract

Pseudomonas syringae pv. tomato (Pst), the causal agent of bacterial speck in tomato, is a model for understanding plant-pathogen coevolution. Within this pathosystem, the emergence of race 1 has traditionally been interpreted as a direct adaptive response to the development of Pto/Prf-mediated resistance in tomato. While race 0 strains are recognized through the type III effectors AvrPto and AvrPtoB, race 1 strains evade this immune surveillance by losing, mutating, or silencing these determinants, thereby overcoming Pto-mediated resistance. However, recent genomic and population-level studies reveal that the evolutionary success of a pathogen lineage extends beyond effector loss alone. Diagnostic progress-from differential host assays to genome-informed tools-has refined race discrimination and revealed the clonal dominance of T1-like lineages worldwide. Comparative genomics has uncovered genetic signatures in race 1, including expanded effector repertoires, plasmid-encoded virulence factors, and an abundance of mobile elements that reflect horizontal gene transfer while simultaneously blurring the boundaries of classical race definitions. These features underpin its capacity for immune evasion, host specialization, and global persistence. Recent outbreaks in Chile, North America, and Europe involving highly aggressive T1-like strains suggest an apparent rise in virulence, yet the drivers of this trend remain unresolved. They likely involve a combination of effector diversification, horizontal gene movement, and environmental or agronomic factors. Understanding these processes will require integrative genomic, transcriptomic, and functional approaches to connect genotype with phenotype. Taken together, revisiting Pst race 1 highlights both the utility and the limitations of race-based classifications and underscores the need for genome-informed surveillance and diversified resistance strategies in tomato breeding. More broadly, race 1 provides a valuable model to explore how agricultural selection and genomic plasticity shape pathogen evolution in crop systems.